After heart attack injury, ALX/FPR2 is activated by resolvin D1 in immune cells in the spleen and in immune cells at the heart attack site. This speeds expedited resolution of the heart attack injury. Researchers now have used mice that completely lack ALX/FPR2 to learn more about the pathways this resolution sensor uses to target inflammation. Such knowledge will help in finding treatments to delay the human heart failure that often follows a heart attack.
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